Bacterial meningitis: complement gene expression in the central nervous system.
Inflammation in the subarachnoid space represents the pathological hallmark of bacterial meningitis. The intrathecal accumulation of leukocytes, in response to bacterial pathogens, and the subsequent release of endogenous inflammatory mediators are associated with a breakdown of the blood-brain barrier function and poor prognosis. Complement has been shown to play a major role in the inflammatory response within the intrathecal compartment in bacterial meningitis. In the present review, we provide an outline of the current understanding of the involvement of the complement system in the pathophysiology of bacterial meningitis, and propose future directions of investigation.
Stahel
P F
PF
Department of Microbiology, University of Alabama at Birmingham 35294, USA.
Barnum
S R
SR
D000706:Anaphylatoxins / Q000276:immunology; D000818:Animals; D001812:Blood-Brain Barrier / Q000276:immunology; D016923:Cell Death / Q000276:immunology; D002490:Central Nervous System / Q000276:immunology* / Q000473:pathology; D003167:Complement Activation / Q000235:genetics / Q000276:immunology*; D003165:Complement System Proteins / Q000235:genetics* / Q000276:immunology; D015870:Gene Expression; D006801:Humans; D016920:Meningitis, Bacterial / Q000235:genetics / Q000276:immunology*; D009693:Nucleic Acid Hybridization; D012333:RNA, Messenger / Q000096:biosynthesis; D011951:Receptors, Complement / Q000037:antagonists & inhibitors
D000706:Anaphylatoxins; D012333:RNA, Messenger; D011951:Receptors, Complement; D003165:Complement System Proteins